By 10 to 14 days of postnatal life ventricular cells from hamsters which model hereditary cardiomyopathy (BIO 14.6 strain) exhibit a hypersensitivity to the Beta -adrenergic agonist isoproterenol. Isoproterenol abnormally prolongs the duration of the cardiomyopathic action potential. This is the earliest in development that a pathophysiological symptom has been disclosed in this disease model. The objective of this study is to explore the mechanism underlying the catecholamine elicited disturbance in electrogenicity of young myopathic sarcolemma, and to learn more of its relationship to the calcium overload that is thought to precipitate spontaneous cellular necrosis that marks the first overtly degenerative stage of the disease. As the balance of trans-sarcolemmal calcium and potassium currents determines the duration of the cardiac action potential, the study focuses on examining these ionic currents by voltage clamping single enzymatically isolated cells (cardiomyocytes). Electrophysiological properties of diseased cells are contrasted with those of normal cells from hearts of a control strain of randomly bred hamsters (BIO RB). Cardiomyocytes isolated from left ventricular tissue of 10 to 15 day old animals are first subjected to standard intracellular electrophysiology for monitoring the condition of action potentials and their responsiveness to varying doses of catecholamines. This is followed with a more detailed analysis of ionic currents with single electrode voltage clamping. These analyses are repeated on progressively younger cells in an effort to resolve the earliest postnatal age that catecholamine hypersensitivity can be observed.